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Darwin’s peppered myth: Turns out, peppered moths take care to protect themselves

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A Darwin cult (the peppered myth) developed during the twentieth century around the peppered moths, with the recent “resounding triumph” that it turns out that pollution effects do favour dark coloured moths over light coloured ones in the same species, with no important changes.

Whoop whoop. That is all Darwinism can come up with, in real life, after all this time.

But so? Snowbelt effects explain why the Canadian Groundhog Day groundhog is white and the American one is brown. No evolution was ever harmed in the making of the diverting nonsense.

In “Peppered Moths Without Evolution” (July 31, 2012), Creation-Evolution Headlines comments , noting a recent, more detailed study,

Kettlewell and Majerus didn’t take into account the moths’ behavior. They treated moths as passive creatures that would alight on tree trunks at random. They placed the selective power in the environment, with lower contrast producing greater camouflage, leaving the high-contrast moths vulnerable to birds.

The South Korean researchers found, instead, that moth behavior plays a vital role in the camouflage. They “found out that moths are walking on the tree bark until they settle down for resting; the insects seem to actively search for a place and a body position that makes them practically invisible.” A video clip embedded in the article shows the moths doing this.

The article avoids superstitious homage to Darwin as well, apparently. That’s a start  in the right direction.

We always thought that the moth had more interest in protecting its hide than the researchers did, and guess what? But how do the moths know if, when they feel invisible, they really are invisible?

See also: US Darwinists (US ranked 14th) wail over South Korea (ranked 1st), supposedly “not able to compete”

Comments
wd400: When you say something like this:
All I said from the start that this was a simple Mendelian trait that arose by mutation then spread rapidly through the population. This is precisely what is seen in the paper
---you're basically saying almost nothing. I guess you don't see that. Either something is transmitted via epigenetics, or, as has been shown recently, absolutely transmitted outside of nuclear DNA, or, it is inherited via nuclear DNA in Mendelian fashion. We're just finding out about these other ways of passing on cellular information. But, if something happens within an organism, and it affects nuclear DNA, or mt-DNA, for that matter, and is inherited in the traditional manner, then, according to your position, this is Darwinian---plain and simple. Well, this covers almost everything. It leaves out little. And so, it says almost nothing. How, is this informative? Mendelian genetics has been known for over a hundred years. No one disputes this. What evolutionary biologists need to demonstrate is that the mechanisms by which "mutations" (another 'catch-all' term among so many others) occur in organisms, occur in such a way as to bring about large scale changes; and, to demonstrate, as well, that these mutations are, indeed, 'random.' You need a lot more than: "If something happens in an organism, and it's inherited, this proves Darwin was right, and that neo-Darwinian analysis is cogent." To equate a TE in the midst of an intron with a SNP--and you do this, since you don't make a distinction[cf. the blocked out quote above]---is an incredible position to take. That's why this thread has been revived. This is NOT the kind of mutation you, or any other evol. biol., had in mind. You just need to admit this. But, you won't budge. Fine. The dust-heap of history awaits.
Even HSP example doesn’t generate adaptive mutations at a greater rate.
This comment flies in the face of the article I cited. I just don't understand your statement. +++++++++++++++++++ You know, one time, when I was working as an engineer, and we were logging an oil well in Beverly Hills, the logging runs kept stopping. This happened a few times. It was a brand new type of log, and it was very costly time wise and otherwise. Now, I found myself in the midst of the logging experts, who had used this logging machine many times before. It was their logging truck we were sitting in. I noticed that it was about the same amount of elapsed time each time before the equipment just shut down. So, after the second run, I began timing the runs. I timed the next two runs. They were exactly the same amount of time. So, I turned to the "experts," and said: "It's the same amount of time each time. It's probably the electric breaker. Do you have a back-up breaker." They said, "Yes, we do." Well, we ran it the third time; this time using the back-up. No problems. Point of the story: We need to learn from our mistakes. We need to 'smell out' the right answer. But, then there's orthodoxy that gets in the way. Right? The guys who worked for the company who invented the logging device could have said: "You don't know anything about this logging device. Leave it to us "experts" to solve." But they didn'tPaV
November 28, 2016
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SA, apparently 'evolution is undeniably true' is the axiom that Darwinists start out with in their theory. The truthfulness of Darwinian evolution is not a conclusion that they have reached by experiment. The truthfulness of evolution is simply never questioned by Darwinists:
Response to John Wise – October 2010 Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism. http://www.evolutionnews.org/2010/10/response_to_john_wise038811.html "One century of studies on mutations has not provided a single verified example of a gene mutation that led to adaptive morphological change in metazoans. (Cabej 2012) Mutation + Selection = Stasis - October 8th, 2014 Excerpt: As a trained physicist, Desai applied a statistical perspective using robots to precisely manipulate hundreds of lines of yeast to perform large scale evolutionary experiments. Scientists have long studied genetic evolution of microbes, but until now, only a few strains at a time. Robotically managing 640 lines of yeast from a single parent cell, Desai’s team was efficiently tooled to statistically analyze evolution at this level for the first time. In an interview with Singer, Joshua Plotkin, an evolutionary scientist at the University of Pennsylvania, commented, “This is the physicist’s approach to evolution, stripping down everything to the simplest possible conditions… They could partition how much of evolution is attributable to chance, how much to the starting point, and how much to measurement noise.”,,, While early mutations in the experiment initially variably influenced fitness, fitness in the final generations was the same. “Scientists,” Singer noted, “don’t know why all genetic roads in yeast seem to arrive at the same endpoint”.,,,, “I think many people think about one gene for one trait, a deterministic way of evolution solving problems,” David Reznick, a biologist at the University of California-Riverside, told Singer. “This says that’s not true.” Unexpectantly, Desai’s team discovered genetic mutations plus selection yields stasis in the microbe model– not evolution. http://www.darwinthenandnow.com/2014/10/mutation-selection-stasis/ Peer-Reviewed Research Paper on Plant Biology Favorably Cites Intelligent Design and Challenges Darwinian Evolution - Casey Luskin December 29, 2010 Excerpt: Many of these researchers also raise the question (among others), why — even after inducing literally billions of induced mutations and (further) chromosome rearrangements — all the important mutation breeding programs have come to an end in the Western World instead of eliciting a revolution in plant breeding, either by successive rounds of selective “micromutations” (cumulative selection in the sense of the modern synthesis), or by “larger mutations” … and why the law of recurrent variation is endlessly corroborated by the almost infinite repetition of the spectra of mutant phenotypes in each and any new extensive mutagenesis experiment instead of regularly producing a range of new systematic species… (Wolf-Ekkehard Lönnig, “Mutagenesis in Physalis pubescens L. ssp. floridana: Some Further Research on Dollo’s Law and the Law of Recurrent Variation,” Floriculture and Ornamental Biotechnology Vol. 4 (Special Issue 1): 1-21 (December 2010).) http://www.evolutionnews.org/2010/12/peer-reviewed_research_paper_o042191.html Dr. Wolf-Ekkehard Lönnig, (retired) Senior Scientist (Biology), Max Planck Institute for Plant Breeding Research, Emeritus, Cologne, Germany.
bornagain77
November 28, 2016
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wd400
Do you know if any of these scenarios would produce the same phenotype, or are you just guessing?
Two of the scenarios I proposed are these: "... any other size more or less?" and "... slightly different location" I could have said actually: "... any different location" When we combine those two variables, we'd have all possible sizes (one to a million?) and all possible locations (unknown huge number). I forgot to add a third variable, not only length but specification of sequence, but anyway. No, I haven't tested all of those yet. But I'd think that would be the task for the evolutionist. We saw nothing about it in the paper. And what if that particular insertion was the only possible scenario that produced the same phenotype? We'd have a one in a trillion, trillion chance or something like that. I'm underestimating. Maybe it's 1 in 10^50 chance or much more? Would that cause you some concern? Would you lose confidence in evolutionary claims? Bacteria to humans. And it took a one in 10^50 mutation just to change pigment on a moths wing. I would hope you'd start questioning the theory at that point. I certainly would.Silver Asiatic
November 28, 2016
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This particular insertion of a 22,000 nucleotide sequence has to qualify as the “very rarely” kind. What if it was only 19,000 nucleotides? Or what if 25,000? Or any other size more or less? What if it was inserted in a slighly different location?
Indeed. Do you know if any of these scenarios would produce the same phenotype, or are you just guessing?wd400
November 28, 2016
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wd's comment @ 86:
No one has ever claimed that that the peppered moths explained “wholesale changes in body-types” – just that they form a nice example of adaptation in a changing environment.
and PaV's excellent response @88 - answered a big question for me in this debate. We don't even have to talk about epigenetics or the non-randomness of transposable elements (as appropriate as it may be). In fact, it might actually help wd's argument if the insertion was driven by epigenetic triggers, because without that we have, in wd's words: "Most of the time these new insertions have no effect, sometimes they create diseases and very rarely the mutation is advantageous." This particular insertion of a 22,000 nucleotide sequence has to qualify as the "very rarely" kind. What if it was only 19,000 nucleotides? Or what if 25,000? Or any other size more or less? What if it was inserted in a slighly different location? It just happens that one conferred an advantage. What kind of probability analysis is (or could be) done on this? But anyway, ok, conceding that it just happened that way, we're still not at the real issue here. We've got a 'very rarely' complex insertion ... and after an incredibly improbable event, what fitness benefit did it confer? Again, as wd explains: "just that they form a nice example of adaptation". That's it. A slight increase melanin - some darker pigmentation in the wing. If that was the end of this evolutionary story, probably most of us would walk away bored and uninterested. But that's not it. That kind of rare insertion, for a change of color in the wings, and at the same time:
PaV: The peppered moth is THE ICON of evolution. And evolution is supposed to tell us how bacteria became humans.
Bacteria to humans. It's easy to forget that's actually what they're claiming. And the peppered moth is evidence for it.Silver Asiatic
November 28, 2016
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Of Note: Dr Hunter has posted his article on ENV:
Peppered Moth: How Evolution's Poster Child Became the Rebuttal - Cornelius Hunter November 27, 2016 Excerpt:,,, The mutating of the protein sequence was the whole idea behind evolution: DNA mutations which lead to changes in a protein can lead to a phenotype change with fitness improvement, and there would be subject to natural selection. That is not what we are seeing in the much celebrated peppered moth example. The DNA mutation is much more complicated (~20,000 nucleotides inserted), and the fact it was inserted into an intron suggests that additional molecular and cellular mechanisms are required for the coloration change to occur. None of this fits evolutionary theory. http://www.evolutionnews.org/2016/11/peppered_moth_h103315.html
bornagain77
November 28, 2016
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Of related note to 173 in regards to 'fitness':
Prehoda's Goof: Mutational Fitness Effects Cannot Be Predicted - November 28, 2016 Excerpt: The new PNAS paper by Bank et al., "On the (un)predictability of a large intragenic fitness landscape," takes a serious look at the effects of mutational interactions.,,, The point of the study is that epistatic interactions are profoundly unpredictable. By performing one of the largest-ever surveys of epistasis on engineered mutations to Hsp90, a well-known protein, they concluded that it is extremely difficult to predict what will happen.,,,their conclusion has far-reaching implications for all evolutionary predictions,,,, "our results highlight the inherent difficulty imposed by the duality of epistasis for predicting evolution. In the absence of epistasis (i.e., in a purely additive landscape), evolution is globally highly predictable because the population will eventually reach the single-fitness optimum, but the path taken is locally entirely unpredictable. Conversely, in the presence of (sign and reciprocal sign) epistasis evolution is globally unpredictable," http://www.evolutionnews.org/2016/11/prehodas_goof_m103316.html
bornagain77
November 28, 2016
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PaV, I don't have time to focus on all of your confused ramblings. So, very briefly... You did indeed claim that the fact this is a TE insertion "proved you right". You have yet to demonstrate why that would be the case. All I said from the start that this was a simple Mendelian trait that arose by mutation then spread rapidly through the population. This is precisely what is seen in the paper. If you want to argue that TE insertion is non-random you'll need some evidence. If you read about TEs you'll see they are inserting themselves all the time, mostly with no effect sometimes creating diseases very rarely being adaptive. You can claim all those adaptive ones are programmed, but there is no reason to imagine this is the case. Even HSP example doesn't generate adaptive mutations at a greater rate. And then you still have the problem that this mutation happened once. What kind of programmed response happens in one of the thousands upon thousands of moths that were subjected to the same stimulus. You are just wrong about to claim that Aboriginal Australians have no genetic link to African populations. I don't know where you got this idea. I guess I thought you were literally talking about "random drift" because you said "random drift". I don't think that's an unreasonable assumption. Finally, the GC rich regions don't have conserved positions in rat and mouse. They graph is made by aligning chunks of the rat genome with the mouse chromosome. You are welcome to google up some more links, misunderstand them, and write a confused rant about them. But I don't think I'll be replying any more.wd400
November 28, 2016
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As I begin my response to your screed, let me remind you that the reason this thread has been raised from the dead is because newly analyzed sequences of Biston betularia, both typica and carboneria, show that it is not a “point mutation” but an TE insert into an ‘intron’ that differentiates the two forms. I stated that this proves me right, and you wrong. Further, I said that if you didn’t admit you were wrong here, you would never admit you were wrong---and, along with you, your fellow evolutionary biologists. All of this only shows that Darwinism is “unfalsifiable” since nothing—no evidence whatsoever---will get you to reconsider the assertions the theory makes.
God, what a load of rubbish.
Just to make sure: you’re not describing evolutionary biology, are you? What you try to convince me and others of is just that: rubbish.
But, again, you are blind to what the actual mechanism causing the insert was. That’s the whole point here. That’s why you’re wrong and I’m right; because all indications are that some internal “engineering” brought this about.
Can we have just one skerrick of evidence for this claim?
This is rich. Is it your claim that, just by chance, a 22,000 nucleotide sequence decided to insert itself, not in an exon---which would mean a protein is modified, but into an “intron,” which will be excised and to evolutionary biologists is no more than “junk DNA.” [That is, termed "junk" until such time that experiments demonstrate that ‘introns’ actually have functions, and play a role in regulation of proteins. Then, you say, well we knew all along that it had some role in regulation. Well, why did you call it junk, then?] All of this happened by chance, you say? Well, give me “one skerrick” of evidence for this claim? Actually, your claim is rubbish. The probablilities are plain against such a thing happening by accident. My claim at least makes some sense. But isn’t that how science is supposed to work? Theory says one thing; something is discovered that makes one question what the theory says, and then a new view of things is conjectured, and then tested. Just like Barbara McClintock did. From the 2014 paper in Chromosoma, “Transposons, environmental changes, and heritable induced phenotypic variability”:
[From the introduction]That data demonstrated that Hsp90 is involved in repression of transposon activity by playing a significant role in piwi-interacting RNA (piRNAs)-dependent RNA interference (RNAi) silencing. The important implication is that the fixed phenotypic abnormalities observed in Hsp90 mutants are probably related to de novo induced mutations by transposon activation. In this case, Hsp90 could be considered as a mutator. . . . [Further down] In other words, evolution is gradual but does not progress at a constant speed. This inconstant speed could be due, at least in part, to the activity of transposons that would act as evolutionary accelerators in the presence of environmental changes. . . . [From the conclusion] Environmental changes, in their ability to induce transposon activation, could be formally considered as both hypermutators and selectors at the same time, leading to an acceleration of the evolutionary process. On the other hand, transposons can be viewed as a trigger of the speciation process through the production of variability and reproductive isolation of new species. This suggests an effective process for rapid evolutionary change and makes it clear why transposons and host genomes, although biological antinomies, have coevolved mechanisms that regulate transposition and mutational outcomes under environmental stress and optimize reciprocal survival in normal environmental conditions. The defense mechanisms and their alterations allow mutual survival of host and mobile elements.
Rubbish, you say?
but, if we know that H. erectus developed into H. sapiens in Africa, and you have a skull that is like H. erectus in Europe and is 700,000 years old, isn’t it entirely possible that it, too, developed into something similar to H. sapiens?
This was literally the multiregional hypothesis that the evidence proved wrong (there have been Homo species out of Africa much longer than 7ka). So, no, it’s not very likely.
And my contention is that your faith in pop. gen. methods is too firm. From the original article I linked to above, I cite the paragraph you were referring to in rebuttal: Today, most academics who have analyzed the Petralona remains say that the cranium of the Archanthropus of Petralona belongs to an archaic hominid distinguished from Homo erectus, and from both the classic Neanderthals and anatomically modern humans, but showing characterists of all those species and presenting strong European traits. A skull dating back 700,000 which is either Homo sapien or part Homo sapien is in direct conflict with the Out of Africa theory of human evolution. It’s either “Homo sapien or part Homo sapien”: that is, it has modern European characteristics. The ‘find’ was denounced, of course. And from a website on “Out of Africa” theories and such:
Out of Asia Theory Some scientists have theorized that an early hominid such as homo habilis left Africa two million years ago and moved into Asia, where it evolved into Homo erectus then spread to Europe and back to Africa. This theory is based on the fact that the Homo erectus specimens found in Asia are older than those found in Africa. Evidence for this theory includes extraordinarily old dates for Homo species that appeared in Indonesia and China just as Homo erectus was emerging in Africa. Berkeley's Carl Swisher told Time magazine that "elephants left Africa several times during their history" and "lots of animals expand their ranges. the main factor may have been an environmental change that made the expansion easier. No other animals needed stone tools to get out of Africa." [Source: Michael Lemonick, Time, March 14, 1994] One primatologist told National Geographic: "The idea that all hominids originated in Africa is a myth created by people working in Africa. Sure, they've found a lot there, but if we'd invested that much time and money in Asia we would find fossil hominids just as old there too." Homo erectus tools have been found in Africa and Europe but not in Asia. Scientists say that the reason for this is that they may have used equally effective bamboo tools--- instead of stone ones---that decay and leave behind no evidence.
A “myth.” Yes, but buttressed by linkage disequilibrium! And I love that final piece: “bamboo tools . . . that decay and leave behind no evidence.” That’s evolution for you: an explanation for what we see, based on what we don’t see. Wonderful! What better science could there be?
I’ll add that I’ve looked around a little, and it seems that the aborigines in Australia have two haplotype clusters (not the 17 in Africa),
This is a prediction of OOA, decreased diversity as you extend from the source population.
Ahah! A prediction! But did it “predict” than no haplotypes whatsoever would be found? Diversity is one thing; absence another.
and that there is good evidence that there is NO African haplotypes found among the Aborigines. So, here’s the question: are Aborigines H.sapiens, or not?
They are. Why do you think the words before this would leave any doubt as to this?
Homo sapiens, per the OOA theory, arose in Africa and then spread. How do you explain the absence of any genetic link to Africa? This seems to bother other scientists.
Use a different word, if you prefer. James Shapiro talks about NGE; so, just think of the “protocol” as an internally guided, and regulated system that responds to environmental stimuli in a generic way, but that through some kind of a feedback system is able to use the cellular mechanisms at its disposal in a genetically targeted way
And do any of these protocols exist, outside of your (and prehaps James Shaprio’s) imagination?
Unfortunately, you have little of it.
As to “drift,” this was just shorthand for organismal mutation rates acting over the entire genome.
You used a term with a precise meaning to describe entirely different than that meaning? And you’re surprised I didn’t get what you were saying?
Why would you think I was literally talking about “random drift.” Had I brought it up before? Now, your response to this would predictably be: “Well, that’s precisely it. You hadn’t brought it up. How was I to understand what you meant?” To which I reply: I was speaking of the probabilities of ”random drift.” Why? Because, in the absence of selection, the probabilities affecting sequences in general are those of random drift. And how can selection work on something that hasn’t arisen yet? Hence, we’re basically dealing with the same prohibitive improbabilities in both cases. Most of us, here at UD, pick up on these things quite easily.
but the paper only demonstrates that SINEs in mice and rats share broad (each point in those graphs represents 2 million base pairs) similarity in preferences for insertion sites, related to the fact they like GC rich sequences and LINEs occupy other regions.
Do you not see that you are making a circular argument. The fact that GC rich sequences have conserved positions is what needs explaining. It’s not the answer; it’s the question.PaV
November 28, 2016
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In another thread wd400 wrote:
"Since fitness is that thing that matters in evolution, that’s something to measure." - wd400 https://uncommondescent.com/intelligent-design/ea-on-random-turtles/#comment-518518
And yet, as we saw in post 170, there is no universally agreed upon measure of fitness:
Fitness: A Battle is Raging The rigor of this approach, however, is lessened because there is as yet no universally agreed upon measure of fitness; fitness is either defined metaphorically, or defined only relative to the particular model or system used. It is fair to say that due to this lack, there is still no real agreement on what exactly the process of natural selection is. This is clearly a problem. https://uncommondescent.com/intelligent-design/survival-of-the-fittest-is-there-really-a-battle-raging-among-evolutionists-over-fitness/
The fact that fitness cannot be accurately measured in any meaningful sense, and therefore rigorously quantified as mathematical a law of nature, is made self-evident by the following:
Op-Ed: Time to Ditch Natural Selection? - Oct. 3, 2015 Excerpt: If NS were a law of nature, we would see every organism trending along the same trajectory: for instance, bearing more offspring. But NS explains opposite outcomes with equal ease (see Oct 1 entry for examples). It explains why the sloth is slow and the cheetah is fast. It explains why the roundworm is round and the flatworm is flat. It explains why some animals bear lots of young and why some bear few. We are led to believe that NS explains up, down, in, out and sideways by some mysterious, aimless force, and whatever results was caused by NS.,,, In journal papers, you can find neo-Darwinians measuring coefficients of selection and using them in differential equations. They speak of positive selection, negative selection, balancing selection, purifying selection, and epigenetic selection. In my experience, this is all hand-waving. It is jargon masquerading as science.,, read more here: http://crev.info/2015/10/op-ed-time-to-ditch-natural-selection/
Moreover, even though 'fitness' figures centrally in the equations of population genetics, 'fitness' actually falsifies Darwinian evolution as a scientific theory. Specifically, in the following video and article, Donald Hoffman has, through numerous computer simulations of population genetics, in which 'fitness' figured centrally in the equations, proved that if Darwinian evolution were actually true then ALL of our perceptions of reality would be illusory.
Donald Hoffman: Do we see reality as it is? – Video – 9:59 minute mark Quote: “,,,evolution is a mathematically precise theory. We can use the equations of evolution to check this out. We can have various organisms in artificial worlds compete and see which survive and which thrive, which sensory systems or more fit. A key notion in those equations is fitness.,,, fitness does depend on reality as it is, yes.,,, Fitness is not the same thing as reality as it is, and it is fitness, and not reality as it is, that figures centrally in the equations of evolution. So, in my lab, we have run hundreds of thousands of evolutionary game simulations with lots of different randomly chosen worlds and organisms that compete for resources in those worlds. Some of the organisms see all of the reality. Others see just part of the reality. And some see none of the reality. Only fitness. Who wins? Well I hate to break it to you but perception of reality goes extinct. In almost every simulation, organisms that see none of reality, but are just tuned to fitness, drive to extinction that perceive reality as it is. So the bottom line is, evolution does not favor veridical, or accurate perceptions. Those (accurate) perceptions of reality go extinct. Now this is a bit stunning. How can it be that not seeing the world accurately gives us a survival advantage?” https://youtu.be/oYp5XuGYqqY?t=601 The Evolutionary Argument Against Reality - April 2016 The cognitive scientist Donald Hoffman uses evolutionary game theory to show that our perceptions of an independent reality must be illusions. Excerpt: “The classic argument is that those of our ancestors who saw more accurately had a competitive advantage over those who saw less accurately and thus were more likely to pass on their genes that coded for those more accurate perceptions, so after thousands of generations we can be quite confident that we’re the offspring of those who saw accurately, and so we see accurately. That sounds very plausible. But I think it is utterly false. It misunderstands the fundamental fact about evolution, which is that it’s about fitness functions — mathematical functions that describe how well a given strategy achieves the goals of survival and reproduction. The mathematical physicist Chetan Prakash proved a theorem that I devised that says: According to evolution by natural selection, an organism that sees reality as it is will never be more fit than an organism of equal complexity that sees none of reality but is just tuned to fitness. Never.” https://www.quantamagazine.org/20160421-the-evolutionary-argument-against-reality/
Although Hoffman tried to limit his results to just our visual perceptions, as Plantinga had pointed out years before Hoffman came along, there is no reason why the results do not also extend to undermining our cognitive faculties as well:
The Case Against Reality - May 13, 2016 Excerpt: Hoffman seems to come to a conclusion similar to the one Alvin Plantinga argues in ch. 10 of Where the Conflict Really Lies: we should not expect — in the absence of further argument — that creatures formed by a naturalistic evolutionary process would have veridical perceptions.,,, First, even if Hoffman’s argument were restricted to visual perception, and not to our cognitive faculties more generally (e.g., memory, introspection, a priori rational insight, testimonial belief, inferential reasoning, etc.), the conclusion that our visual perceptions would be wholly unreliable given natural selection would be sufficient for Plantinga’s conclusion of self-defeat. After all, reliance upon the veridicality of our visual perceptions was and always will be crucial for any scientific argument for the truth of evolution. So if these perceptions cannot be trusted, we have little reason to think evolutionary theory is true. Second, it’s not clear that Hoffman’s application of evolutionary game theory is only specially applicable to visual perception, rather than being relevant for our cognitive faculties generally. If “we find that veridical perceptions can be driven to extinction by non-veridical strategies that are tuned to utility rather than objective reality” (2010, p. 504, my emphasis), then why wouldn’t veridical cognitive faculties (more generally) be driven to extinction by non-veridical strategies that are tuned to utility rather than objective reality? After all, evolutionary theory purports to be the true account of the formation of all of our cognitive faculties, not just our faculty of visual perception. If evolutionary game theory proves that “true perception generally goes extinct” when “animals that perceive the truth compete with others that sacrifice truth for speed and energy-efficiency” (2008), why wouldn’t there be a similar sacrifice with respect to other cognitive faculties? In fact, Hoffman regards the following theorem as now proven: “According to evolution by natural selection, an organism that sees reality as it is will never be more fit than an organism of equal complexity that sees none of reality but is just tuned to fitness” (Atlantic interview). But then wouldn’t it also be the case that an organism that cognizes reality as it is will never be more fit than an organism of equal complexity that cognizes none of reality but is just tuned to fitness? On the evolutionary story, every cognitive faculty we have was produced by a process that was tuned to fitness (rather than tuned to some other value, such as truth). http://www.gregwelty.com/2016/05/the-case-against-reality/
Thus, in what should be needless to say, a worldview that undermines the scientific method itself by holding all our observations of reality, and cognitive faculties, are illusory is NOT a worldview that can be firmly grounded within the scientific method!
Steps of the Scientific Method Observation/Research Hypothesis Prediction Experimentation Conclusion http://www.sciencemadesimple.com/scientific_method.html
Moreover, completely contrary to what Hoffman found for Darwinian theory, it turns out that accurate perception, i.e. conscious observation, of reality, far from being unreliable and illusory, is experimentally found to be far more integral to reality, i.e. far more reliable of reality, than the math of population genetics predicted. In fact, in the following experiment it was found that reality doesn’t exist without an observer.
New Mind-blowing Experiment Confirms That Reality Doesn’t Exist If You Are Not Looking at It – June 3, 2015 Excerpt: The results of the Australian scientists’ experiment, which were published in the journal Nature Physics, show that this choice is determined by the way the object is measured, which is in accordance with what quantum theory predicts. “It proves that measurement is everything. At the quantum level, reality does not exist if you are not looking at it,” said lead researcher Dr. Andrew Truscott in a press release.,,, “The atoms did not travel from A to B. It was only when they were measured at the end of the journey that their wave-like or particle-like behavior was brought into existence,” he said. Thus, this experiment adds to the validity of the quantum theory and provides new evidence to the idea that reality doesn’t exist without an observer. http://themindunleashed.org/2015/06/new-mind-blowing-experiment-confirms-that-reality-doesnt-exist-if-you-are-not-looking-at-it.html
Apparently science itself could care less if atheists are forced to believe, because of the mathematics of population genetics, that their observations of reality, and cognitive faculties, are illusory! Verse:
2 Peter 1:16 For we have not followed cunningly devised fables, when we made known unto you the power and coming of our Lord Jesus Christ, but were eyewitnesses of his majesty.
bornagain77
November 27, 2016
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wd
Well, as I’ve said many times, the fact this is a mutation that happened in one moth seems to rule out the idea it’s a programmed response. You can always invoke untestable =divine intervention or similar for this one mutation, but there’s not reason to think this one TE insertion was different than the millions of others.
Well, patterns within the moth genome could have been shaped, simultaneously by insertion events like this. We don't know what the mutation rate is or how to model the range of variation we could expect with the number of different sized segments that could be copy/inserted, and the effects they could have. We don't know how improbable this particular advantageous mutation was. But it remains true that we don't know what influenced the mutation (if anything), even if it was a single event.
We know from studies like these that some TEs preferentially insert into genomic regions with a hight proportion of “A”s and “T”s, or near a particular motif, or even into other copies of themselves. Combine that with selection removing from elements that insert into genes and get non-random patterns of TEs in the genome.
That's another area for study and it could be that mutational-biases like this are caused more directly by environmental factors which trigger a clustering of TEs or affect the mutation rate itself. Ok, I don't think we can tie any of that back to this particular study (for one reason, the authors didn't explore it), but I find this to be a much more open question. An 'edited', complex segment of code spliced into a non-coding region, which ultimately drove the morphological variation is a lot more difficult to explain, in probabilistic terms, than a simple point mutation in the coding region. Also, how do we know these events are random with regards to fitness and not, rather, a response of the organism to fitness pressures (and as some claim, the organism adjusts its own DNA in response)?Silver Asiatic
November 27, 2016
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It is interesting to note that if one wants to build a better random number generator for a computer program then a better source of entropy is required to be found to drive the increased randomness:
Cryptographically secure pseudorandom number generator Excerpt: From an information theoretic point of view, the amount of randomness, the entropy that can be generated is equal to the entropy provided by the system. But sometimes, in practical situations, more random numbers are needed than there is entropy available. http://en.wikipedia.org/wiki/Cryptographically_secure_pseudorandom_number_generator
Yet there are two major problems, for the materialist, with entropy being found to be the primary source of randomness in the universe. The first problem is that Entropy is the most finely tuned initial condition of the universe, and Entropy is also governed by a constant.
The Physics of the Small and Large: What is the Bridge Between Them? Roger Penrose Excerpt: "The time-asymmetry is fundamentally connected to with the Second Law of Thermodynamics: indeed, the extraordinarily special nature (to a greater precision than about 1 in 10^10^123, in terms of phase-space volume) can be identified as the "source" of the Second Law (Entropy)." http://irafs.org/irafs_1/cd_irafs02/texts/penrose.pdf Bruce Gordon, PhD math, discusses the initial entropy of the universe in this following video The Multiverse confirms the Ontological Argument for God https://www.youtube.com/watch?v=MgDn_k11ups&t=12s The Austrian physicist Ludwig Boltzmann first linked entropy and probability in 1877. However, the equation as shown, involving a specific constant, was first written down by Max Planck, the father of quantum mechanics in 1900. In his 1918 Nobel Prize lecture, Planck said: This constant is often referred to as Boltzmann’s constant, although, to my knowledge, Boltzmann himself never introduced it – a peculiar state of affairs, which can be explained by the fact that Boltzmann, as appears from his occasional utterances, never gave thought to the possibility of carrying out an exact measurement of the constant. Nothing can better illustrate the positive and hectic pace of progress which the art of experimenters has made over the past twenty years, than the fact that since that time, not only one, but a great number of methods have been discovered for measuring the mass of a molecule with practically the same accuracy as that attained for a planet. http://www.daviddarling.info/encyclopedia/B/Boltzmann_equation.html
Thus the randomness inherent in the Entropy of the universe is actually proof for Theism and is not proof for Atheism, as the materialist apparently falsely believes in his appeal to randomness. The second major problem, for the materialist, is that Entropy, i.e. the universal tendency of things to decay towards disorder, almost directly contradicts the claims of Darwinists that increases in functional complexity/information/order can easily be had. IOW, not only does Evolution not have any known universal law to appeal to, as other overarching theories of science have, the second law of thermodynamics, i.e. Entropy, a law with great mathematical explanatory power in science, almost directly contradicts Darwinian claims that increases in functional complexity/information can be easily had:
Why Tornados Running Backward do not Violate the Second Law – Granville Sewell – May 2012 – article with video Excerpt: So, how does the spontaneous rearrangement of matter on a rocky, barren, planet into human brains and spaceships and jet airplanes and nuclear power plants and libraries full of science texts and novels, and supercomputers running partial differential equation solving software , represent a less obvious or less spectacular violation of the second law—or at least of the fundamental natural principle behind this law—than tornados turning rubble into houses and cars? Can anyone even imagine a more spectacular violation? https://uncommondescent.com/intelligent-design/why-tornados-running-backward-do-not-violate-the-second-law/ “Gain in entropy always means loss of information, and nothing more.” Gilbert Newton Lewis – preeminent Chemist of the first half of last century
Thus, the materialist's appeal to 'uncaused randomness' to try to get around Theism backfires on the materialist since, number 1, Entropy, i.e. the source for randomness in the universe, is proof for Theism not atheism, and 2, the type of 'decaying randomness' inherent in Entropy is completely antithetical to the claims of Darwinists that increasing complexity and order are supposedly easy to achieve: Verse and quote:
Psalm 102:25-27 Of old You laid the foundation of the earth, And the heavens are the work of Your hands. They will perish, but You will endure; Yes, they will all grow old like a garment; Like a cloak You will change them, And they will be changed. But You are the same, And Your years will have no end. "We have the sober scientific certainty that the heavens and earth shall ‘wax old as doth a garment’.... Dark indeed would be the prospects of the human race if unilluminated by that light which reveals ‘new heavens and a new earth.’" Sir William Thomson, Lord Kelvin (1824 – 1907) – pioneer in many different fields, particularly electromagnetism and thermodynamics.
bornagain77
November 27, 2016
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wd400 at 165 and elsewhere states:
"random with respect to fitness"
Just don't ask for a precise, mathematically useful, quantification of 'fitness'
Fitness: A Battle is Raging The rigor of this approach, however, is lessened because there is as yet no universally agreed upon measure of fitness; fitness is either defined metaphorically, or defined only relative to the particular model or system used. It is fair to say that due to this lack, there is still no real agreement on what exactly the process of natural selection is. This is clearly a problem. http://telicthoughts.com/fitness-a-battle-is-raging/#more-7550
Although wd400 has used the weasel term 'random with respect to fitness' a few times in this thread, and elsewhere, to try to dodge the evidence that mutations are being directed in the genome, (such as this following evidence),,
Rapid Evolution of Citrate Utilization by Escherichia coli by Direct Selection Requires citT and dctA. - Minnich - Feb. 2016 The isolation of aerobic citrate-utilizing Escherichia coli (Cit(+)) in long-term evolution experiments (LTEE) has been termed a rare, innovative, presumptive speciation event. We hypothesized that direct selection would rapidly yield the same class of E. coli Cit(+) mutants and follow the same genetic trajectory: potentiation, actualization, and refinement. This hypothesis was tested,,, Potentiation/actualization mutations occurred within as few as 12 generations, and refinement mutations occurred within 100 generations.,,, E. coli cannot use citrate aerobically. Long-term evolution experiments (LTEE) performed by Blount et al. (Z. D. Blount, J. E. Barrick, C. J. Davidson, and R. E. Lenski, Nature 489:513-518, 2012, http://dx.doi.org/10.1038/nature11514 ) found a single aerobic, citrate-utilizing E. coli strain after 33,000 generations (15 years). This was interpreted as a speciation event. Here we show why it probably was not a speciation event. Using similar media, 46 independent citrate-utilizing mutants were isolated in as few as 12 to 100 generations. Genomic DNA sequencing revealed an amplification of the citT and dctA loci and DNA rearrangements to capture a promoter to express CitT, aerobically. These are members of the same class of mutations identified by the LTEE. We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved. http://www.ncbi.nlm.nih.gov/pubmed/26833416 Michael Behe's Quarterly Review of Biology Paper Critiques Richard Lenski's E. Coli Evolution Experiments - December 2010 Excerpt: After reviewing the results of Lenski's research, Behe concludes that the observed adaptive mutations all entail either loss or modification--but not gain--of Functional Coding ElemenTs (FCTs) http://www.evolutionnews.org/2010/12/michael_behes_quarterly_review041221.html Evolution of an Irreducibly Complex System – Lenski’s E. Coli – Feb. 2015 Conclusion: When viewed objectively, without the blinders of materialistic philosophy, Lenski’s experiments are strong evidence for, and a powerful vindication of, Behe’s arguments in particular, and the skeptics of Darwinism in general. At the end of the day, Lenski’s E. coli are just another in a long line of Darwinian claims that, upon closer inspection, fail to live up to their hype: from moth coloration to finch beaks to antibiotic resistance in bacteria. In each case, when these examples are carefully studied, instead of supporting the grander claims of the evolutionary creation story, they inadvertently demonstrate the pathetic impotence of Darwinian mechanisms and underscore the need for an alternative source of innovation in the history of life. https://uncommondescent.com/irreducible-complexity/evolution-of-an-irreducibly-complex-system-lenskis-e-coli/#comment-551158
,,, Although wd400 has used the weasel term 'random with respect to fitness' a few times in this thread to try to dodge the evidence presented to him that mutations are being directed in the genome, the fact of the matter is that random mutations are central to Darwinian thinking. Moreover, this randomness postulate of materialists, at least the way materialists use it, is indistinguishable from the Theist's own appeal to a miracle.
Evolution and the Illusion of Randomness - Talbott - Fall 2011 Excerpt: The situation calls to mind a widely circulated cartoon by Sidney Harris, which shows two scientists in front of a blackboard on which a body of theory has been traced out with the usual tangle of symbols, arrows, equations, and so on. But there’s a gap in the reasoning at one point, filled by the words, “Then a miracle occurs.” And the one scientist is saying to the other, “I think you should be more explicit here in step two.” In the case of evolution, I picture Dennett and Dawkins filling the blackboard with their vivid descriptions of living, highly regulated, coordinated, integrated, and intensely meaningful biological processes, and then inserting a small, mysterious gap in the middle, along with the words, “Here something random occurs.” This “something random” looks every bit as wishful as the appeal to a miracle. It is the central miracle in a gospel of meaninglessness, a “Randomness of the gaps,” demanding an extraordinarily blind faith. At the very least, we have a right to ask, “Can you be a little more explicit here?” http://www.thenewatlantis.com/publications/evolution-and-the-illusion-of-randomness
Wolfgang Pauli comments on the shell game that Darwinists play with the word ‘chance’ here
Pauli’s ideas on mind and matter in the context of contemporary science – Harald Atmanspacher Excerpt: “In discussions with biologists I met large difficulties when they apply the concept of ‘natural selection’ in a rather wide field, without being able to estimate the probability of the occurrence in a empirically given time of just those events, which have been important for the biological evolution. Treating the empirical time scale of the evolution theoretically as infinity they have then an easy game, apparently to avoid the concept of purposesiveness. While they pretend to stay in this way completely ‘scientific’ and ‘rational,’ they become actually very irrational, particularly because they use the word ‘chance’, not any longer combined with estimations of a mathematically defined probability, in its application to very rare single events more or less synonymous with the old word ‘miracle.’” Wolfgang Pauli (pp. 27-28) http://www.igpp.de/english/tda/pdf/paulijcs8.pdf
Robert C. Sproul points out: “By calling the unknown cause ‘chance’ for so long, people begin to forget that a substitution was made. . . . The assumption that ‘chance equals an unknown cause’ has come to mean for many that ‘chance equals cause.’”
The Universal Determinism Dichotomy (UDD) - David L. Abel - 2015 Excerpt: We sometimes appeal to yet-to-be-discovered laws when trying to explain what appears to be chance phenomena. Most theorists, however, attempt to reduce Chance Contingency to unknown and/or very complex physical causation, as summarized by Peale.12 Thus Chance Contingency as a true cause may be only “apparent.” Sproul argues effectively that chance is not a cause of anything. Chance is nothing more than a statistical description of unknown or complex physical causation. Chance, therefore, cannot have any physical effects, since it is not a physical cause. 13,,, 13. Sproul RC. - Not a Chance: the Myth of Chance in Modern Science and Cosmology. Grand Rapids, MI: Baker Books; 1994 https://www.academia.edu/12267097/The_Universal_Determinism_Dichotomy_UDD_
Thus to say a mutation “happened randomly by chance', as it is usually used by Darwinists, is in reality a 'placeholder for ignorance' instead of being an appeal to a known cause. Thus, when an atheist states that something happened by chance, we have every right to ask, as Talbott pointed out, “Can you be a little more explicit here?” Nobel laureate Jacques L. Monod, for one, used this chance-equals-cause line of reasoning.
“Pure chance, absolutely free but blind, [is] at the very root of the stupendous edifice of evolution,” Monod wrote. “Man knows at last that he is alone in the universe’s unfeeling immensity, out of which he emerged only by chance.”
‘By chance' Monod does what many other materialists do—he elevates chance to a creative principle that is indistinguishable from the Theist’s own appeal to a miracle. Chance, as it is used by materialists, is, in fact, offered as a 'God substitute' by materialists as the 'uncaused cause' by which the universe and by which all life on earth came to be. Moreover, if we try be 'a little more explicit here' as Talbott stated, then we find that the 'randomness postulate' of materialists falls apart upon closer examination.bornagain77
November 27, 2016
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God, what a load of rubbish.
But, again, you are blind to what the actual mechanism causing the insert was. That’s the whole point here. That’s why you’re wrong and I’m right; because all indications are that some internal “engineering” brought this about.
Can we have just one skerrick of evidence for this claim?
but, if we know that H. erectus developed into H. sapiens in Africa, and you have a skull that is like H. erectus in Europe and is 700,000 years old, isn’t it entirely possible that it, too, developed into something similar to H. sapiens?
This was literally the multiregional hypothesis that the evidence proved wrong (there have been Homo species out of Africa much longer than 7ka). So, no, it's not very likely.
I’ll add that I’ve looked around a little, and it seems that the aborigines in Australia have two haplotype clusters (not the 17 in Africa),
This is a prediction of OOA, decreased diversity as you extend from the source population.
and that there is good evidence that there is NO African haplotypes found among the Aborigines. So, here’s the question: are Aborigines H.sapiens, or not?
They are. Why do you think the words before this would leave any doubt as to this?
Use a different word, if you prefer. James Shapiro talks about NGE; so, just think of the “protocol” as an internally guided, and regulated system that responds to environmental stimuli in a generic way, but that through some kind of a feedback system is able to use the cellular mechanisms at its disposal in a genetically targeted way
And do any of these protocols exist, outside of your (and prehaps James Shaprio's) imagination?
As to “drift,” this was just shorthand for organismal mutation rates acting over the entire genome.
You used a term with a precise meaning to describe entirely different than that meaning? And you're surprised I didn't get what you were saying?
Sternberg points out that the positions have been “preserved.” So, you’re problem is explaining why the positions are “preserved” from rats to mice.
I'm not sure what you mean by preserved, but the paper only demonstrates that SINEs in mice and rats share broad (each point in those graphs represents 2 million base pairs) similarity in preferences for insertion sites, related to the fact they like GC rich sequences and LINEs occupy other regions.wd400
November 26, 2016
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wd400:
You don’t need much pop gen to understand the evidence for a single origin: why would the allele be so closely associated with a particular genetic background if it had been generated by multiple separate mutations?
Are you trying to tell me that if there were 10, or 20, or even thirty, with this new mutation, and they began to interbreed, that you could tell the difference in 2010? Hard to believe. But, again, you are blind to what the actual mechanism causing the insert was. That's the whole point here. That's why you're wrong and I'm right; because all indications are that some internal "engineering" brought this about.
Out of Africa refers to Homo sapiens even your alternative archeology site doesn’t claim this skull is from our species.
Well, if the skull is from 700,000 years ago, then why would it be H.sapien? Here's the problem you need to address: if homo sapiens came "out of africa" and then diversified, where did the "europeoid" features come from? I guess you could say that there was some kind of "human" ( homo') population in Europe that the Africa H. sapiens mixed with; but, if we know that H. erectus developed into H. sapiens in Africa, and you have a skull that is like H. erectus in Europe and is 700,000 years old, isn't it entirely possible that it, too, developed into something similar to H. sapiens? I'll add that I've looked around a little, and it seems that the aborigines in Australia have two haplotype clusters (not the 17 in Africa), and that there is good evidence that there is NO African haplotypes found among the Aborigines. So, here's the question: are Aborigines H.sapiens, or not? Or, maybe, as I saw in one paper criticizing the OOA Theory: it's a premise "based on a mixture of statistics and best guesses.”
What “protocols”, who said anything about drift?
Use a different word, if you prefer. James Shapiro talks about NGE; so, just think of the "protocol" as an internally guided, and regulated system that responds to environmental stimuli in a generic way, but that through some kind of a feedback system is able to use the cellular mechanisms at its disposal in a genetically targeted way. Just use your imagination. Darwin said that biologists of his day didn't have enough imagination. Maybe it's still true. As to "drift," this was just shorthand for organismal mutation rates acting over the entire genome. I thought for sure you would understand the shorthand. You know: the standard ID argument for the implausibility of specific mutations. (The answer comes back: "Oh, but because of "random drift," somewhere in the population the 'mutation' already exists." You see, Darwinism is never wrong. It just can't be.)
SINEs tend to insert in GC rich sequences, and not into LINEs. If composition of the chromosomes are conserved you may well get SINEs inserting into the same windows in each genome.
Sternberg points out that the positions have been "preserved." So, you're problem is explaining why the positions are "preserved" from rats to mice.PaV
November 26, 2016
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PaV, You don't need much pop gen to understand the evidence for a single origin: why would the allele be so closely associated with a particular genetic background if it had been generated by multiple separate mutations? For the rest of this little survey of tangentially related factoids: Out of Africa refers to Homo sapiens even your alternative archeology site doesn't claim this skull is from our species. I can't find anything resembling meaning in this passage
[Further, I proposed a mechanism above that involved random mutations, but a mechanism, nevertheless, that is part of the organism’s cellular “protocol.” Hence, the probabilities fall well outside that, let’s say, of random drift.] What "protocols", who said anything about drift? I'll read the ENV link, but it wouldn't surprise me that there was coarse similarity in SINE insertion sites among mice and rats. SINEs tend to insert in GC rich sequences, and not into LINEs. If composition of the chromosomes are conserved you may well get SINEs inserting into the same windows in each genome.
wd400
November 26, 2016
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wd400: Well, as I’ve said many times, the fact this is a mutation that happened in one moth seems to rule out the idea it’s a programmed response. You can always invoke untestable =divine intervention or similar for this one mutation, but there’s not reason to think this one TE insertion was different than the millions of others. You don't know that the 'mutation' happened in "one moth": you're presuming that based on your confidence in population genetics. And here, your confidence in pop gen is 'linked' to evidence from "linkage disequilibrium." That is, the haplotypes they make reference to in the Naturearticle we are now discussing from June of this year, are what are identified and used when using linkage disequilibrium techniques. Yet, there is the example of the entire "Man Out of Africa" Theory---(modern man moved up from Africa about 200,000 ya, and then diversified. [We know this, BTW, because of the presence of a "bottleneck". Remember our discussion about that years ago?]). This theory is based on linkage disequilibrium and, yet, just recently, a European human skull was found in a cave that dates to 700,000 ya.
The ‘Petralona man’, or Archanthropus of Petralona, as it has since been called, was found to be 700,000 years old, making it the oldest human europeoid (presenting European traits) of that age ever discovered in Europe. Dr Poulianos’ research showed that the Petralona man evolved separately in Europe and was not an ancestor of a species that came out of Africa.
Oops!! How many times have I said that you are way too confident of the techniques of pop gen. But, even granting that the date is right; and even granting that it was "one moth" that inserted the TE, you still have no way in the world to rule out whether this was brought about epigenetically or not. This reality is completely blind to the techniques you rely on. [Further, I proposed a mechanism above that involved random mutations, but a mechanism, nevertheless, that is part of the organism's cellular "protocol." Hence, the probabilities fall well outside that, let's say, of random drift.] If you want to insist that linkage disequilibrium somehow assures you of this, then I would respond that our discussion on "bottlenecks" (where you never sufficiently responded to my critique that "bottlenecks" are blind because of the way they are defined, and that they could be hundreds of thousands of years off) and now the results of 'linkage disequilibrium,' or shall I say the known failure of the technique in terms of human ancestry, should give pause to anyone who takes it seriously. I was just looking at this article by Richard Sternberg at ENV about SINE's, and their positioning between rats and mice. Guess what, the SINES on a particular chromosome line up. I think you would do well to read it.PaV
November 26, 2016
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SA, Well, as I've said many times, the fact this is a mutation that happened in one moth seems to rule out the idea it's a programmed response. You can always invoke untestable =divine intervention or similar for this one mutation, but there's not reason to think this one TE insertion was different than the millions of others. These other quotes turn on different meanings of "random". We know from studies like these that some TEs preferentially insert into genomic regions with a hight proportion of "A"s and "T"s, or near a particular motif, or even into other copies of themselves. Combine that with selection removing from elements that insert into genes and get non-random patterns of TEs in the genome. But that doesn't mean TE insertion is random with respect to fitness, which is the important point.wd400
November 26, 2016
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wd400
You can read up yourself, but as I said insertion is what TEs do. We don’t know enough about these moths to know the rate of insertion per generation, but in other species there can be multiple insertions per generation.
The dispute here is whether this particular TE was a single, random insertion or whether it was triggered by some cue or is part of some other non-random process. From a paper BA77 quoted on TEs in plants:
The results show that each family of elements is preferentially integrated in one specific fraction of its respective host genome. This demonstrates that the distribution of transposable elements in the nuclear genome of plants is not random but compartmentalized ...
So, there's evidence of non-randomness here. Why not the same in the moth genome? Are you too quick to declare it a single random event without further analysis?Silver Asiatic
November 26, 2016
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As to unexpected 'non-random' patterns, Sternberg has this article
Discovering Signs in the Genome by Thinking Outside the BioLogos Box - Richard Sternberg - March 17, 2010 Excerpt: The scale on the x-axis is the same as that of the previous graph--it is the same 110,000,000 genetic letters of rat chromosome 10. The scale on the y-axis is different, with the red line in this figure corresponding to the distribution of rat-specific SINEs in the rat genome (i.e., ID sequences). The green line in this figure, however, corresponds to the pattern of B1s, B2s, and B4s in the mouse genome.... *The strongest correlation between mouse and rat genomes is SINE linear patterning. *Though these SINE families have no sequence similarities, their placements are conserved. *And they are concentrated in protein-coding genes.,,, ,,, instead of finding nothing but disorder along our chromosomes, we are finding instead a high degree of order. Is this an anomaly? No. As I'll discuss later, we see a similar pattern when we compare the linear positioning of human Alus with mouse SINEs. Is there an explanation? Yes. But to discover it, you have to think outside the BioLogos box. http://www.evolutionnews.org/2010/03/signs_in_the_genome_part_2032961.html Beginning to Decipher the SINE Signal - Richard Sternberg - March 18, 2010 Excerpt: So for a pure neutralist model to account for the graphs we have seen, ~300,000 random mutation events in the mouse have to match, somehow, the ~300,000 random mutation events in the rat. What are the odds of that? http://www.evolutionnews.org/2010/03/beginning_to_decipher_the_sine032981.html
bornagain77
November 26, 2016
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Origenes, darwinspredictions.com can now be accessed here: https://sites.google.com/site/darwinspredictions/homebornagain77
November 26, 2016
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wd400: Hunter said to generate this mutation would require “inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome”. Well, we know that is happening all the time. TEs copy (or cut and paste) themselves into new positions in the genome all the time. Most of the time these new insertions have no effect, sometimes they create diseases and very rarely the mutation is advantageous.
You are implying that these insertions are random, which would be consistent with your non-teleological Darwinian expectations. Dr. Hunter wrote in 2009:
… new findings are now revealing more about how rice can rapidly adapt. In this case the smart adaptations were caused by transposable elements which are small segments of DNA that evolutionists thought inconveniently plopped themselves down in the genome whereever they happened to land. The transposable elements would help only rarely when a lucky insertion occurred.
In post #122 Bornagain77 provides several references to studies which show that transposon insertion is not a random event. Dr. Hunter’s point is straightforward and simple: transposable elements increases the search space, and all you have done so far is ignore this irrefutable fact. Here it is again:
… evolutionary theory requires that the needed random DNA mutational change is reasonably likely to occur. Given the moth’s effective population size, the moth’s generation time period, and the complexity of the mutation, the needed mutation is not likely to occur. Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome. This is an enormous space of mutational possibilities to search through. It doesn’t add up. Evolution does not have the resources in terms of time and effective population size to come anywhere close to searching this astronomical mutational space. It’s not going to happen. [Dr. Hunter]
------ p.s. Dr.Hunter’s website darwinspredictions.com has been hacked.Origenes
November 26, 2016
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“inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome” is exactly what TEs do.
This is similar to the following “discussion”: X: IPhones arise by sheer dumb luck. Y: You must be mistaken, because an IPhone arising by sheer dumb luck would be a very unlikely event. X: Not at all. We see IPhones everywhere.
I think if you reflect on this you'll see there is really no relation between the two. To make it simpler -- Hunter said to generate this mutation would require "inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome". Well, we know that is happening all the time. TEs copy (or cut and paste) themselves into new positions in the genome all the time. Most of the time these new insertions have no effect, sometimes they create diseases and very rarely the mutation is advantageous.wd400
November 25, 2016
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On the unfalsifiable pseudo-scientific nature of Darwinian evolution: As far as having a rigid mathematical basis to test against as other overarching theories of science have, Darwinian evolution is a untestable, and therefore unfalsifiable, pseudo-science, whereas, on the other hand, Intelligent Design is very much a testable, and therefore falsifiable, science since it is based on the rigid math within 'conservation of information' theorems (Dembski; Marks). https://uncommondescent.com/biology/coming-soon-design-disquisitions-a-new-id-blog/#comment-620985 Of related note: In so far as Darwinian evolution is dependent on the premises of reductive materialism, (which I would argue Darwinism is absolutely dependent on the premises of reductive materialism), and regardless of whether Darwinists ever personally accept the falsification or not, Darwinian evolution is now empirically falsified by advances in quantum biology. Specifically, reductive materialism cannot explain the ‘non-local’, beyond space and time, effect of quantum entanglement/information in molecular biology:
"What happens is this classical information (of DNA) is embedded, sandwiched, into the quantum information (of DNA). And most likely this classical information is never accessed because it is inside all the quantum information. You can only access the quantum information or the electron clouds and the protons. So mathematically you can describe that as a quantum/classical state." Elisabeth Rieper – Classical and Quantum Information in DNA – video (Longitudinal Quantum Information resides along the entire length of DNA discussed at the 19:30 minute mark; at 24:00 minute mark Dr Rieper remarks that practically the whole DNA molecule can be viewed as quantum information with classical information embedded within it) https://youtu.be/2nqHOnVTxJE?t=1176 Molecular Biology – 19th Century Materialism meets 21st Century Quantum Mechanics – video https://www.youtube.com/watch?v=rCs3WXHqOv8 Looking beyond space and time to cope with quantum theory – 29 October 2012 Excerpt: “Our result gives weight to the idea that quantum correlations somehow arise from outside spacetime, in the sense that no story in space and time can describe them,” http://www.quantumlah.org/highlight/121029_hidden_influences.php Quantum correlations do not imply instant causation – August 12, 2016 Excerpt: A research team led by a Heriot-Watt scientist has shown that the universe is even weirder than had previously been thought. In 2015 the universe was officially proven to be weird. After many decades of research, a series of experiments showed that distant, entangled objects can seemingly interact with each other through what Albert Einstein famously dismissed as “Spooky action at a distance”. A new experiment by an international team led by Heriot-Watt’s Dr Alessandro Fedrizzi has now found that the universe is even weirder than that: entangled objects do not cause each other to behave the way they do. http://phys.org/news/2016-08-quantum-imply-instant-causation.html
i.e. Quantum information is experimentally shown to be a non-local', beyond space and time, effect that is irreducible to reductive materialistic explanations. And as such, since Darwinian evolution is based on reductive materialistic premises, then Darwinian evolution is experimentally falsified as the scientific explanation for molecular biology. Moreover, I would also argue, along with Penrose and Hameroff, that this non-local quantum information provides physical evidence that is very suggestive for the existence of the 'soul':
“Let’s say the heart stops beating. The blood stops flowing. The microtubules lose their quantum state. But the quantum information, which is in the microtubules, isn’t destroyed. It can’t be destroyed. It just distributes and dissipates to the universe at large. If a patient is resuscitated, revived, this quantum information can go back into the microtubules and the patient says, “I had a near death experience. I saw a white light. I saw a tunnel. I saw my dead relatives.,,” Now if they’re not revived and the patient dies, then it's possible that this quantum information can exist outside the body. Perhaps indefinitely as a soul.” - Stuart Hameroff - Quantum Entangled Consciousness - Life After Death - video (5:00 minute mark) https://youtu.be/jjpEc98o_Oo?t=300 LIFE AFTER DEATH: Shock claim of evidence showing consciousness may continue as a SOUL THE human conscious lives on after death, scientists have sensationally claimed. By Sean Martin - Sun, Nov 6, 2016 Excerpt: Sir Roger states if a person temporarily dies, this quantum information is released from the microtubules and into the universe. However, if they are resuscitated the quantum information is channeled back into the microtubules and that is what sparks a near death experience. Sir Roger added: “If they’re not revived, and the patient dies, it’s possible that this quantum information can exist outside the body, perhaps indefinitely, as a soul.” http://www.express.co.uk/news/science/728897/LIFE-AFTER-DEATH-consciousness-continue-SOUL
What Penrose and Hameroff are referring to is the fact that in quantum mechanics it is quantum information that is primarily conserved, and not necessarily energy and matter that are primarily conserved, as energy and matter are primarily conserved in classical mechanics: (November 2016) https://uncommondescent.com/intelligent-design/philosopher-of-science-roger-penrose-thinks-soul-may-survive-death/#comment-620372bornagain77
November 25, 2016
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wd400: Per the piece you keep quoting, “inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome” is exactly what TEs do.
This is similar to the following "discussion":
X: IPhones arise by sheer dumb luck. Y: You must be mistaken, because an IPhone arising by sheer dumb luck would be a very unlikely event. X: Not at all. We see IPhones everywhere.
Origenes
November 25, 2016
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correction: You might want to reflect on how desperately you are keeping Darwin's’s scenario alive in some form. There all better.
False Darwinian prediction: Mutations are not adaptive - Cornelius Hunter Excerpt: The second problem is that organisms use strategies to direct the mutations according to the threat. Adaptive mutations have been extensively studied in bacteria. Experiments typically alter the bacteria food supply or apply some other environmental stress causing mutations that target the specific environmental stress. (Burkala, et. al.; Moxon, et. al; Wright) Adaptive mutations have also been observed in yeast (Fidalgo, et. al.; David, et. al.) and flax plants. (Johnson, Moss and Cullis) One experiment found repeatable mutations in flax in response to fertilizer levels. (Chen, Schneeberger and Cullis) Another exposed the flax to four different growth conditions and found that environmental stress can induce mutations that result in “sizeable, rapid, adaptive evolutionary responses.” (Chen, Lowenfeld and Cullis) In response to this failed prediction some evolutionists now are saying that evolution somehow created the mechanisms that cause mutations to be adaptive. https://sites.google.com/site/darwinspredictions/mutations-are-not-adaptive
bornagain77
November 25, 2016
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Epicycles it is then! You might want to reflect on how desperately you are keeping Hunter's scenario alive in some form. Like, how greatly does this programmed response present in all moths (your words...) happening in one clutch of eggs improve the odds compared to it happening in one moth? And remember these moths are diploid and reproduce sexually, so there are at least 4 haplotypes surrounding the insertion site in any clutch and two in each offspring. So, do even make this tiny improvement to the odds of Hunter's scenario you need to explain why the mutation happened in only one of these backgrounds. As I say, i encourage you to take a step back, stop trying to defend someone simply because they propose an idea you'd like to be true and engage with the data. Per the piece you keep quoting, "inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome" is exactly what TEs do.wd400
November 25, 2016
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wd400: You can keep constructing epicycles to support Hunter’s idea (like, why would any moths share such a long haplotype in the original population ...
Didn't I mention (#149) that a female moth lays about 2,000 eggs? So, why is this in any way unlikely?
wd400: ... let alone why only those moths with this long haplotype of mostly neutral variants would produce this mutation…)
It is your assumption that these variants are neutral. They may very well not be neutral wrt the insertion. Anyway, this is your selective skepticism speaking.
wd400: ... or try to engage with the data in an attempt to understand it rather than prop an idea that you prefer. It’s really up to you.
Indeed. Let's do just that. Which brings us back to Dr.Hunter:
Dr. Hunter: … evolutionary theory requires that the needed random DNA mutational change is reasonably likely to occur. Given the moth’s effective population size, the moth’s generation time period, and the complexity of the mutation, the needed mutation is not likely to occur. Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome. This is an enormous space of mutational possibilities to search through. It doesn’t add up. Evolution does not have the resources in terms of time and effective population size to come anywhere close to searching this astronomical mutational space. It’s not going to happen. [dr. Hunter]
Origenes
November 25, 2016
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"You can keep constructing epicycles" spits coffee out laughing!,,,
A Philosophical Question…Does Evolution have a Hard Core ? Some Concluding Food for Thought Excerpt: So basically, the demarcation problem is a fun game philosophers enjoy playing, but when they realize the implications regarding the theory of evolution, they quickly back off… http://www.samizdat.qc.ca/cosmos/philo/hardcore_pg.htm
Imre Lakatos, although he tipped toed around the failure of Darwinism to have a rigid demarcation criteria in science, he was brave enough to state that a good scientific theory will make successful predictions in science and a pseudo-scientific theory will generate ‘epicycle theories’ to cover up embarrassing failed predictions.
“In degenerating programmes, however, theories are fabricated only in order to accommodate known facts” – Imre Lakatos (November 9, 1922 – February 2, 1974) a philosopher of mathematics and science, , quote as stated in 1973 LSE Scientific Method Lecture
And on that score, Darwinism squarely qualifies as a pseudo-science:
"When their expectations turn out to be false, evolutionists respond by adding more epicycles to their theory that the species arose spontaneously from chance events. But that doesn’t mean the science has confirmed evolution as Velasco suggests. True, evolutionists have remained steadfast in their certainty, but that says more about evolutionists than about the empirical science." ~ Cornelius Hunter Here’s That Algae Study That Decouples Phylogeny and Competition - June 17, 2014 Excerpt: "With each new absurdity another new complicated just-so story is woven into evolutionary theory. As Lakatos explained, some theories simply are not falsifiable. But as a result they sacrifice realism and parsimony." - Cornelius Hunter http://darwins-god.blogspot.com/2014/06/heres-that-algae-study-that-decouples.html "Being an evolutionist means there is no bad news. If new species appear abruptly in the fossil record, that just means evolution operates in spurts. If species then persist for eons with little modification, that just means evolution takes long breaks. If clever mechanisms are discovered in biology, that just means evolution is smarter than we imagined. If strikingly similar designs are found in distant species, that just means evolution repeats itself. If significant differences are found in allied species, that just means evolution sometimes introduces new designs rapidly. If no likely mechanism can be found for the large-scale change evolution requires, that just means evolution is mysterious. If adaptation responds to environmental signals, that just means evolution has more foresight than was thought. If major predictions of evolution are found to be false, that just means evolution is more complex than we thought." ~ Cornelius Hunter
Following in Lakatos's footsteps, Dr. Hunter has compiled a list of some of the major false predictions generated by evolutionary theory that Darwinists have to make excuses for. False predictions that are fundamental to evolutionary theory, i.e. go to the ‘core’ of the theory, as it were, and falsify it from the inside out using Lakatos’s demarcation criteria.
Darwin’s (failed) Predictions – Cornelius G. Hunter – 2015 This paper evaluates 23 fundamental (false) predictions of evolutionary theory from a wide range of different categories. The paper begins with a brief introduction to the nature of scientific predictions, and typical concerns evolutionists raise against investigating predictions of evolution. The paper next presents the individual predictions in seven categories: early evolution, evolutionary causes, molecular evolution, common descent, evolutionary phylogenies, evolutionary pathways, and behavior. Finally the conclusion summarizes these various predictions, their implications for evolution’s (in)capacity to explain phenomena, and how they bear on evolutionist’s claims about their theory. https://sites.google.com/site/darwinspredictions/home
And here is a broader overview of the many failed predictions of naturalism/materialism, in comparison to the many successful predictions of Theism, in regards to the major scientific discoveries that have now been revealed by modern science:
Theism compared to Materialism/Naturalism – a comparative overview of the major predictions of each philosophy – video https://youtu.be/QQ9iyCmPmz8
Verse:
1 Thessalonians 5:21 but test everything; hold fast what is good.
bornagain77
November 25, 2016
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You can keep constructing epicycles to support Hunter's idea (like, why would any moths share such a long haplotype in the original population, let alone why only those moths with this long haplotype of mostly neutral variants would produce this mutation...) or try to engage with the data in an attempt to understand it rather than prop an idea that you prefer. It's really up to you.wd400
November 25, 2016
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